Abstract
Osteoarthritis (OA) is a degenerative chronic disease that affects various tissues surrounding the joints, such as the subchondral bone and articular cartilage. The onset of OA is associated with uncontrolled catabolic and anabolic remodeling processes of the joints, including the cartilage and subchondral bone, to adapt to local biological and biochemical signals. In this study, we determined whether 70% ethanolic (EtOH) extract of Litsea japonica fruit (LJFE) had beneficial effects on the articular cartilage, including structural changes in the tibial subchondral bone, matrix degradation, and inflammatory responses, in OA by using a rat model of monosodium iodoacetate-induced OA. Our results showed that administration of LJFE increased the bone volume and cross-section thickness, but the mean number of objects per slice in this group was lower than that in the OA control (OAC) group. In addition, the LJFE decreased the expression of inflammatory cytokines. Compared to the OAC group, the group treated with high doses of LJFE (100 and 200 mg/kg) showed a more than 80% inhibition of the expression of matrix metalloproteinases and tissue inhibitors of metalloproteinases. Our results suggest that LJFE can be used as a potential anti-osteoarthritic agent.
Highlights
Osteoarthritis (OA) is a degenerative disease and is a major cause of disability and pain, especially in the elderly population [1]
Hamabiwalactone A and B present in the L. japonica fruit may be used as active ingredients for the treatment of OA, and in this study, we measured the levels of hamabiwalactone A and B in the LJFE
To determine whether LJFE may affect the destruction of articular cartilage, we examined the expression of the OA biomarkers matrix metalloproteinases (MMPs)-2, MMP-3, MMP-7, MMP-9, MMP-13, tissue inhibitor of metalloproteinases (TIMPs)-1, and TIMP-2 in the articular cartilage of MIAinduced OA rats
Summary
Osteoarthritis (OA) is a degenerative disease and is a major cause of disability and pain, especially in the elderly population [1]. OA is characterized by the progressive loss of articular cartilage and formation of osteophytes and is associated with degeneration of the cartilage and changes to the subchondral bone, which lead to chronic pain and functional limitations in the joint [3,4]. Degradation of the articular cartilage in OA is mediated by excessive synthesis and release of catabolic and inflammatory factors such as matrix metalloproteinases (MMPs), tissue inhibitor of metalloproteinases (TIMPs), and cytokines [5]. MMPs play an important role in tissue remodeling and in destruction of the cartilage and bone in arthritic joints [6]. Cartilage degradation in OA is recognized to be induced by inflammatory cytokines such as interleukin-6 (IL-6), IL-1β, and tumor necrosis factor-α (TNF-α) [9]. MMPs, TIMPs, and inflammatory cytokines are reasonable therapeutic approaches for the treatment of OA [8]
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